The more rapid effector T cell migration to the site of infection in BALB/c mice may allow for the early expression of IL-4Rα-dependent anti-helminth effector molecules typically associated with the protective response in challenge infection with H. p. bakeri. In challenged mice, Th2 cells, eosinophils, and M2 macrophages rapidly accumulate around the developing larvae inhibiting their development in an IgG1- and arginase-1 (Arg-1)-dependent manner via L-arginine depletion36–38. This evidence concerns the gene IL4R and infection.